Tick-borne encephalitis virus and the immune response of the mammalian host

被引：64

作者：

Doerrbecker, Bastian ^{[1
]}

Dobler, Gerhard ^{[2
]}

Spiegel, Martin ^{[1
]}

Hufert, Frank T. ^{[1
]}

机构：

[1] Univ Med Ctr, Dept Virol, D-37075 Gottingen, Germany

[2] Inst Microbiol Armed Forces, D-80937 Munich, Germany

来源：

TRAVEL MEDICINE AND INFECTIOUS DISEASE | 2010年 / 8卷 / 04期

关键词：

Tick-borne encephalitis (TBE); Tick-borne encephalitis virus (TBEV); Mammalian immune system; Innate and adaptive immunity; INTERFERON-PRODUCING CELLS; TERM-FOLLOW-UP; DENDRITIC CELLS; WEST-NILE; JAPANESE ENCEPHALITIS; VIRAL-INFECTION; TRANSGENIC MICE; CLINICAL-COURSE; CEREBROSPINAL-FLUID; LANGERHANS CELLS;

D O I：

10.1016/j.tmaid.2010.05.010

中图分类号：

R1 [预防医学、卫生学];

学科分类号：

1004 ; 120402 ;

摘要：

Tick-borne encephalitis (TBE) is caused by Tick-borne encephalitis virus (TBEV), one of the most prevalent arboviruses in Europe and in many parts of Asia. Transmission of TBEV to humans usually occurs by bite of an infected tick or rarely by ingestion of unpasteurized milk products of infected livestock. TBEV infection induces an innate and adaptive immune response, nevertheless it is able to replicate in several cell types of the immune system at the same time which probably contributes to the spread of the virus in the human host. Furthermore, TBEV can enter the central nervous system (CNS) by yet not well understood mechanisms via the blood brain barrier (BBB) or the olfactory neurons which leads to serious neurological disorders like meningitis, encephalitis or even meningoencephalitis. In this article we review the known facts and possible hypotheses of interaction of TBEV with components of the mammalian immune system and their implications for TBEV-mediated pathogenesis. (C) 2010 Elsevier Ltd. All rights reserved.

引用

页码：213 / 222

页数：10

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